Ketone bodies mediate alterations in brain energy metabolism and biomarkers of Alzheimer's disease.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic pathways and existing biomarker studies without primary data or systematic review methodology.
PubMed 38033541 · doi:10.3389/fnins.2023.1297984
What was done
This narrative review summarizes published literature on how ketone bodies, generated via fatty acid beta-oxidation through ketogenic diets, influence brain energy metabolism in Alzheimer's disease (AD). It details the physiological mechanisms of ketone utilization during brain glucose hypometabolism and compiles evidence regarding the effects of ketogenic interventions on AD fluid biomarkers (Aβ, p-tau-181, GFAP, NFL), neuroinflammation, oxidative stress, and mitochondrial function.
What was found
The abstract reports no quantitative data, effect sizes, or study counts. It notes qualitatively that reduced brain glucose metabolism and mitochondrial dysfunction emerge up to 15 years prior to clinical AD onset, that ketone bodies cross the blood-brain barrier to provide alternative fuel, and outlines literature connecting ketogenic diets to alterations in AD fluid biomarkers and neuroinflammatory pathways.
Why it matters
Synthesizes the biological rationale and emerging biomarker evidence for using ketogenic interventions to bypass cerebral glucose deficits in neurodegenerative disease.
Limits
As a narrative review, it presents no original empirical data, uses no systematic search protocol, and does not provide quantitative synthesis or risk-of-bias evaluation for the discussed studies.
Cited by
- supports In Alzheimer's disease, the brain's capacity to metabolize and utilize glucose declines.